A working model for the mechanisms of actin dynamics during dendritic spine development. (1) Spine development starts with the initiation of the dendritic filopodium and its elongation. At this stage, the filopodia are highly dynamic, undergoing continuous elongation and shrinking. We propose that mDia2 promotes actin filament polymerization in the filopodium tip. The factors driving actin filament polymerization in the roots of filopodia remains to be identified. (2) The spine head begins to form. We propose that the mechanism of actin assembly is gradually changed from an mDia2-mediated polymerization of unbranched actin filaments to an Arp2/3-nucleated branched actin filament network, leading to enlargement of the spine head. The spine heads are highly dynamic, continuously changing their shape, and long protrusions from the spine heads are frequently seen. We propose that the function of ADF/cofilins, in addition to replenishing the cytoplasmic actin monomer pool in neurons, is to control the proper length of actin filaments and thus to prevent formation of abnormal protrusions from spine heads. Future studies will be required to reveal the exact spine locations where ADF/cofilins are active. (3) Mature spines are still dynamic but maintain their overall morphology. Dynamics occur as small protrusions on the surface of the spine head (morphing).